This invention relates generally to methods and apparatus for Diagnostic Imaging (DI), and more particularly to methods and apparatus that provide for 3D and 2D relative perfusion viability.
When a patient comes into an emergency room or other clinical setting and is being evaluated for a possible heart attack there are usually three possible outcomes concerning myocardial health. 1. No disease (and a doctor is not going to treat the patient), 2. Positive disease (minor disease, and the doctor will typically treat with medication(s)), and 3. Positive disease (major disease, and the doctor typically treats with revascularization such as Coronary Artery Bypass Grafting (CABG) or angioplasty (AP)).
A simple Computed Tomography (CT) angiography can determine if there is no disease present. However, additional information is needed to determine the severity of the disease if disease is present.
CT uses both anatomical and functional methods to determine the perfusion and viability of the myocardium. CT also provides functional information about flow through microvasculature within the myocardium imaging following the injection of a contrast agent. This allows for the visualization of the perfusion or blood flow through regions of myocardium that may be affected. Regions lacking microvasculature flow show up as hypo-enhancement due to the lack of contrast agent flowing through that area. The large or moderate perfusion defects can be measured using nuclear imaging, but also can be evaluated with greater resolution using a simple low dose technique. This technique is based on the uptake of the contrast agent in the myocardium. Normal myocardium shows a more rapid uptake of contrast agent with a fairly rapid washout. The slightly damaged and less perfused tissue will gradually reach maximum uptake of contrast agent. However, there will be a time differential between the normal myocardium and the slightly injured myocardium. The more injured myocardium will never have maximum uptake of contrast agent due to lack of perfusion and it will take a greater amount of time to washout.
Additionally, a technique called delayed hyper-enhancement CT can be employed to reveal the extent of injured myocardium in dysfunctional myocardial tissue, hence the capability of recovering contractile function once blood flow delivering oxygen and substrates is restored, either spontaneously or following revascularization. In delayed hyper-enhancement, an additional agent is infused either continuously or as a bolus via an intravenous route and an image is taken 10-15 minutes following infusion. In normal myocardium, the infused contrast agent is excluded from intracellular compartments, however, in injured myocardium, the sarcolemmal membrane of myocytes become permeable allowing contrast agent to accumulate, which results in the observed hyper-enhancement. Thus, lack of contractile function (hypokinesia) and absence of hyper-enhancement (preserved integrity of the sarcolemmal membrane of myocytes) may indicate the presence of hibernating myocardium, which is likely to improve after revascularization of the artery supplying that particular territory. CT imaging using the above, described combination of anatomical and functional methods may reliably differentiate areas of hibernating (viable) from infracted (non-viable) myocardium following a heart attack.
Measuring the signal intensity changes allows one to evaluate for a possible perfusion deficit or hyper-enhancement, thereby indicating abnormal tissue.
When one images the myocardium, the peak uptake of the normal myocardium, which is measured by the timing bolus, there is the greatest differential between normal myocardium and damaged myocardium. For those pixels that have an intensity level in an overlap region as explained in greater detail below, the clustering algorithm herein described helps to discriminate which bin it belongs to. In other words, an isolated pixel or two in the overlap region may not be statistically significant.